『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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登録内容 (EID=140323)

EID=140323EID:140323, Map:0, LastModified:2012年8月30日(木) 15:13:28, Operator:[大家 隆弘], Avail:TRUE, Censor:0, Owner:[松本 満], Read:継承, Write:継承, Delete:継承.
種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
招待 (推奨):
審査 (推奨): Peer Review [継承]
カテゴリ (推奨):
共著種別 (推奨):
学究種別 (推奨):
組織 (推奨): 1.分子酵素学研究センター (〜2007年3月31日/->組織[疾患酵素学研究センター]) [継承]
著者 (必須): 1. (英) Hoshino Katsuaki (日) (読)
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2. (英) Sugiyama Takahiro (日) (読)
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3.松本 満 ([徳島大学.先端酵素学研究所.重点研究部門])
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[継承]
4. (英) Tanaka Takashi (日) (読)
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[継承]
5. (英) Saito Masuyoshi (日) (読)
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[継承]
6. (英) Hemmi Hiroaki (日) (読)
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[継承]
7. (英) Ohara Osamu (日) (読)
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[継承]
8. (英) Akira Shizuo (日) (読)
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9. (英) Kaisho Tsuneyasu (日) (読)
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[継承]
題名 (必須): (英) IκB kinase-α is critical for interferon-α production induced by Toll-like receptors 7 and 9  (日)    [継承]
副題 (任意):
要約 (任意): (英) The Toll-like receptor (TLR) family has important roles in microbial recognition and dendritic cell activation. TLRs 7 and 9 can recognize nucleic acids and trigger signalling cascades that activate plasmacytoid dendritic cells to produce interferon-alpha (IFN-alpha) (refs 7, 8). TLR7/9-mediated dendritic cell activation is critical for antiviral immunity but also contributes to the pathogenesis of systemic lupus erythematosus, a disease in which serum IFN-alpha levels are elevated owing to plasmacytoid dendritic cell activation. TLR7/9-induced IFN-alpha induction depends on a molecular complex that contains a TLR adaptor, MyD88, and IFN regulatory factor 7 (IRF-7) (refs 10-14), but the underlying molecular mechanisms are as yet unknown. Here we show that IkappaB kinase-alpha (IKK-alpha) is critically involved in TLR7/9-induced IFN-alpha production. TLR7/9-induced IFN-alpha production was severely impaired in IKK-alpha-deficient plasmacytoid dendritic cells, whereas inflammatory cytokine induction was decreased but still occurred. Kinase-deficient IKK-alpha inhibited the ability of MyD88 to activate the Ifna promoter in synergy with IRF-7. Furthermore, IKK-alpha associated with and phosphorylated IRF-7. Our results identify a role for IKK-alpha in TLR7/9 signalling, and highlight IKK-alpha as a potential target for manipulating TLR-induced IFN-alpha production.  (日)    [継承]
キーワード (推奨): 1. (英) Adaptor Proteins, Signal Transducing (日) (読) [継承]
2. (英) Animals (日) (読) [継承]
3. (英) Cells, Cultured (日) (読) [継承]
4. (英) Cytokines (日) (読) [継承]
5. (英) Dendritic Cells (日) (読) [継承]
6. (英) I-kappa B Kinase (日) (読) [継承]
7. (英) Interferon-alpha (日) (読) [継承]
8. (英) Mice (日) (読) [継承]
9. (英) Myeloid Differentiation Factor 88 (日) (読) [継承]
10. (英) Phosphorylation (日) (読) [継承]
11. (英) Promoter Regions, Genetic (日) (読) [継承]
12. (英) Toll-Like Receptor 7 (日) (読) [継承]
13. (英) Toll-Like Receptor 9 (日) (読) [継承]
14. (英) Up-Regulation (日) (読) [継承]
発行所 (推奨):
誌名 (必須): Nature ([Nature Publishing Group])
(pISSN: 0028-0836, eISSN: 1476-4687)

ISSN (任意): 1476-4687
ISSN: 0028-0836 (pISSN: 0028-0836, eISSN: 1476-4687)
Title: Nature
Title(ISO): Nature
Publisher: Nature Publishing Group
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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年月日 (必須): 西暦 2006年 4月 初日 (平成 18年 4月 初日) [継承]
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DOI (任意): 10.1038/nature04641    (→Scopusで検索) [継承]
PMID (任意): 16612387    (→Scopusで検索) [継承]
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評価値 (任意): **** [制限]
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備考 (任意): 1.(英) Article.Affiliation: Laboratory for Host Defense, RIKEN Research Center for Allergy and Immunology, Suehiro-cho 1-7-22, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]
3.(英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't  (日)    [継承]

標準的な表示

和文冊子 ● Katsuaki Hoshino, Takahiro Sugiyama, Mitsuru Matsumoto, Takashi Tanaka, Masuyoshi Saito, Hiroaki Hemmi, Osamu Ohara, Shizuo Akira and Tsuneyasu Kaisho : IκB kinase-α is critical for interferon-α production induced by Toll-like receptors 7 and 9, Nature, Vol.440, No.7086, 949-953, 2006.
欧文冊子 ● Katsuaki Hoshino, Takahiro Sugiyama, Mitsuru Matsumoto, Takashi Tanaka, Masuyoshi Saito, Hiroaki Hemmi, Osamu Ohara, Shizuo Akira and Tsuneyasu Kaisho : IκB kinase-α is critical for interferon-α production induced by Toll-like receptors 7 and 9, Nature, Vol.440, No.7086, 949-953, 2006.

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